Reversal of reentry and acceleration due to double-wave reentry: two mechanisms for failure to terminate tachycardias by rapid pacing.

OBJECTIVES: We sought to demonstrate mechanisms by which rapid pacing can cause conduction block without terminating reentry. BACKGROUND: Rapid pacing can fail to terminate or can accelerate tachycardias in patients. Mechanisms for these responses are poorly understood. METHODS: We studied reentry in the canine atrial tricuspid ring and a left ventricular ring in vitro in 12 preparations. Activations were recorded from 10 sites around the ring, and monophasic action potentials were recorded from critical sites of block. Rapid pacing at cycle lengths that intermittently caused conduction block was performed at multiple sites. RESULTS: Action potential alternans contributed to block of an orthodromic impulse during rapid pacing. When pacing continued for two stimuli after orthodromic block, a second episode of block could reverse the direction of tachycardia. Continued pacing at this site was likely to produce block of an antidromic impulse, which may initiate double-wave reentry. Double-wave reentry could be sustained or nonsustained. Its cycle length was 56% to 77% of the single-wave cycle length. The ratio of double-wave cycle length to single-wave cycle length was inversely correlated with the relative excitable gap (p < 0.01). Double-wave reentry can be a mechanism for persistent cycle length alternation during tachycardia. CONCLUSIONS: Successful termination of reentry by rapid pacing required block of an othrodromic impulse and stopping pacing within one stimulus after orthodromic block. Reversal of reentry makes the circuit resistant to termination from this site of pacing. Antidromic block can cause acceleration due to double-wave reentry when there is a substantial excitable gap.

Circadian pattern of ventricular tachyarrhythmias in patients with implantable cardioverter-defibrillators.

OBJECTIVES: This study examined the temporal patterns of ventricular tachycardia detections by implantable cardioverter-defibrillators for circadian variability. BACKGROUND: Previous studies of circadian arrhythmia patterns have been methodologically limited by very brief observational periods. Late-generation implantable cardioverter-defibrillators accurately record the times of arrhythmia detections during unlimited follow-up. METHODS: Forty-three patients with late-generation implantable cardioverter-defibrillators were followed up for 226 +/- 179 days (mean +/- SD). The times of all recorded episodes of ventricular tachyarrhythmias were retrieved from the data log of each device during follow-up. RESULTS: The weighted distribution of 830 ventricular tachyarrhythmia episodes from the 43 patients fit a single harmonic sine curve model with a peak between 2 and 3 P.M. (95% confidence interval 1:13 to 4:13 P.M., R = 0.75, p < 0.05). The distributions of spontaneously terminating episodes, episodes receiving device therapy, episodes receiving shocks and episodes in the absence of antiarrhythmic therapy also fit the sine curve model (all R = 0.53 and 0.73, all p < 0.05), all with peak frequencies between 2:08 and 3:09 P.M. and 95% confidence intervals for peak frequencies between 11:38 A.M. and 5:07 P.M. Episodes recorded during continuous antiarrhythmic drug therapy did not fit the model (p > 0.05). CONCLUSIONS: The distribution of ventricular tachyarrhythmias detected by late-generation implantable cardioverter-defibrillators follows a circadian pattern, with a peak tachycardia frequency between noon and 5 P.M. This pattern was not observed in patients receiving antiarrhythmic drug therapy. Knowledge of circadian periodicity for these events has implications for patient management.

Sensing lead-related complications in patients with transvenous implantable cardioverter-defibrillators.

The widespread use of the redesigned Endotak lead (CPI, St. Paul, Minnesota), which combines transvenous pacing, sensing, and defibrillation on a single transvenous lead in patients receiving transvenous implantable cardioverter-defibrillators (ICDs), has reduced morbidity and shortened length of hospital stay after ICD implantation. We describe the incidence and management of Endotak sensing lead-related failures in a series of 348 consecutive patients from 4 institutions who underwent implantation between 1990 and 1995. We retrospectively reviewed the databases for patients receiving an ICD with an Endotak lead for the incidence of lead-related sensing abnormalities. Ten patients (2.8%) with lead-related sensing abnormalities were detected at a mean of 15 +/- 11 months after ICD implantation. Sensing abnormalities were detected in 6 patients after they received inappropriate shocks. Noise or oversensing was noted in 7 patients from interrogation of the devices' data logs. Eight patients had a new transvenous sensing lead placed, 1 patient had a new Endotak lead placed, and 1 had a chronic pacemaker sensing lead converted to function as a sensing lead. No further sensing problems were noted in 8 of 10 patients during a mean follow-up of 14 +/- 8 months. The site of the sensing lead failure was localized to the subrectus pocket in 5 patients and to the clavicle-first rib area in 3 patients; it was undetermined and presumed to be in the clavicle-first rib area in the other 2 patients. One patient had late failure of the defibrillation lead. We conclude that Endotak sensing lead failure does not require insertion of a new Endotak lead, but can be managed with close follow-up and insertion of a new transvenous sensing lead. Endotak lead fractures are frequently localized to the ICD pocket.

Ventricular reentry around a fixed barrier. Resetting with advancement in an in vitro model.

We studied an in vitro model of reentrant tachycardia in a ring of ventricular endocardial tissue surrounding the canine mitral and aortic valves to understand how the response of a reentrant tachycardia to premature impulses can provide insight into the underlying tachycardia mechanism, circuit characteristics, and nature of the central barrier. Reproducible regular reentrant tachycardias (cycle length range, 177-450 msec) were induced with programmed stimulation in 19 intact preparations studied at 34-38 degrees C. Tachycardias were sustained and stable until terminated by programmed stimulation in 95% of preparations. Reentry was reliably reinitiated during experiments lasting 2-15 hours. Data supporting reentry as the mechanism of these tachycardias included sequential activation around the ring that spanned the cycle length of the tachycardia, unidirectional block during initiation of the reentrant rhythm, and termination of the tachycardia after interruption of the circuit. Tachycardias in 13 preparations were systematically reset by premature stimuli. During reentry, each of these preparations had full recovery of excitability by the end of their excitable gap as evidenced by a flat portion along their resetting response curve (eight of 13) or by lack of faster conduction velocity during the second poststimulus beat after premature impulses that produced a long return cycle (13 of 13). From analysis of the conduction of premature impulses and their return cycles, we reached several conclusions useful for interpreting resetting response curves when the reentrant circuit is not fully accessible for study. The duration of a flat portion of the resetting response curve indicated the duration of the shortest fully recovered excitable gap in the reentrant circuit. The window of reset of the tachycardia reflected only the local excitable gap at the site of stimulation and did not define the shortest excitable gap within the circuit. The extent of advancement of the tachycardia provided a lower-limit estimate of the shortest excitable gap in the reentrant circuit. Advancement of a tachycardia in time by premature stimuli indicated advancement at each point in the circuit. Finally, for tachycardias advanced by premature impulses, the length of the reentrant path cannot be determined by the recovery of a refractory barrier.

Coronary artery bypass surgery in patients on chronic hemodialysis. A case-control study.

STUDY OBJECTIVE: To determine the morbidity and mortality of cardiac catheterization and coronary artery bypass surgery in patients on chronic hemodialysis. DESIGN: Retrospective case-control study. SETTING: A referral-based university hospital. PATIENTS: Sixteen consecutive patients on chronic hemodialysis who had catheterization and bypass surgery: 30 controls matched for age, sex, year of operation, severity of coronary disease, left ventricular function, hypertension, diabetes, and urgency of surgery: and 34 consecutive controls having bypass surgery. MEASUREMENTS AND MAIN RESULTS: No major complications of catheterization occurred. Of 16 patients on dialysis, 7 had urgent surgery within 24 hours of catheterization. One patient on dialysis and 3 consecutive controls died, but none of the matched controls died. Postoperative morbidity was increased in the hemodialysis group as measured by the duration of mechanical ventilation (4.7 +/- 2.3 compared with 1.5 +/- 0.8 days in matched controls [mean +/- SE]), the duration of hemodynamic support (4.2 +/- 2.3 compared with 0.8 +/- 0.2 days), the length of stay in the intensive care unit (6.4 +/- 2.4 compared with 2.8 +/- 0.9 days), and the length of postoperative stay in the hospital (15.4 +/- 2.1 compared with 10.8 +/- 1.1 days) (all P less than 0.05). Four intraoperative myocardial infarctions occurred in patients on dialysis compared with two patients in the case-matched controls. Differences in morbidity between the two control groups were not significant. CONCLUSIONS: Morbidity is increased in patients on hemodialysis having coronary artery bypass surgery compared with controls matched for severity of coronary disease; however, the outcome in all but one patient on dialysis was good. Bypass surgery is an acceptable treatment for patients on dialysis with advanced coronary artery disease. Because urgent surgery is often needed in these patients, earlier evaluation of the need for revascularization may improve clinical results.

Long-term temporal patterns of ventricular tachyarrhythmias.

BACKGROUND: Technological limitations have precluded investigation of long-term temporal patterns of ventricular tachyarrhythmia recurrences. Newer implantable cardioverter-defibrillators permit such analyses by accurately recording the time and date of tachycardia detections during long-term follow-up. This study tests the hypothesis that ventricular tachycardia occurrences are randomly distributed over time in individual patients. METHODS AND RESULTS: The time and date of 727 episodes of ventricular tachyarrhythmias were recorded from the data logs of 31 patients with implantable cardioverter-defibrillators followed for a median of 177 days (range, 7 to 782 days). All patients had three or more ventricular tachycardia detections and no detections from causes other than ventricular arrhythmias. In 28 of 31 patients, the distribution of the interdetection time intervals during follow-up differed significantly (all P < .01) from an exponential model distribution of interdetection intervals that assumed that detections were equally likely to occur at any time during follow-up (random). The Kolmogorov-Smirnov goodness-of-fit test was used to compare sample and model distributions. In each patient, the nonrandom distributions resulted from a preponderance of interdetection time intervals that were shorter than predicted by the random model, resulting in a temporal clustering of arrhythmic events. The interdetection interval was < or = 1 hour and < or = 91 hours for 55% and 78% of all intervals, respectively. When only those episodes receiving shock or antitachycardia pacing therapy were analyzed, 25 of 29 patients still manifested nonrandom distributions (all P < .01). When only episodes with tachycardia rates > 240 beats per minute were analyzed, 11 of 13 patients manifested non-random distributions (all P < .01). CONCLUSIONS: Ventricular tachycardia detections and delivered antitachycardia therapies by implantable cardioverter-defibrillators are nonrandomly distributed throughout long-term follow-up in the majority of patients. The temporal clustering of these arrhythmic events may allow preemptive antiarrhythmic therapy and should be considered in the design of therapy based on suppression of spontaneous ventricular arrhythmias to statistically derived end points.

A four-shock Bayesian up-down estimator of the 80% effective defibrillation dose.

INTRODUCTION: New defibrillation techniques are often compared to standard approaches using the defibrillation threshold. However, inference from thresholding data necessitates extrapolation from reactions to relatively ineffective shocks, an error prone procedure requiring large sample sizes for hypothesis testing and large safety margins for defibrillator implantation. In contrast, this article presents a clinically validated statistical model of a minimum error, four-shock defibrillation testing protocol for estimating the 80% effective defibrillation strength for a given patient (ED80). METHODS AND RESULTS: A Bayesian statistical model was constructed assuming that the defibrillation dose-response curve is sigmoidal, and the ED80 is between 150 and 750 V. The model was used to design a minimum predicted error testing protocol and estimates. To prospectively validate the testing protocol and estimates, 170 patients received voltage-programmed biphasic testing. Four fibrillation episodes were induced and terminated in each patient according to the Bayesian up-down protocol. In addition, a validation attempt was made at the estimated ED80 rounded up to the nearest 50 V. In order to estimate the safety margin, in 136 patients, a defibrillation attempt was made at the rounded ED80 + 100 V. Of the 170 attempts at the rounded ED80, 143 (84%) attempts terminated fibrillation. Of the 136 attempts at the rounded ED80 + 100 V, 133 (98%) were effective. CONCLUSIONS: The four-shock Bayesian up-down protocol is the first clinical protocol to accurately predict an ED80 voltage. A 100 V increment above the ED80 provides an adequate safety margin. This simple and accurate method for estimating a highly effective defibrillation dose may be a valuable tool for population-based clinical hypothesis testing, as well as defibrillator implantation.